Objective. To reveal the expression profile of miRNA in glioma and the effects of microRNA-339-5p (miR-339-5p) on glioma. Methods. The glioma and normal tissues were randomly selected for miRNA gene chip detection and qRT-PCR verification. The U87 cells were separated into miR-NC, miR-339-5p mimic, and miR-339-5p suppressor group. Clonogenesis test, flow cell technique, Transwell, and cell scratch assay were utilized to verify the roles of miR-339-5p in cell proliferation, cell apoptosis, cell invasion, and cell migration. The epithelial-meso-transformation-associated proteins was verified by Western blot. Results. A total of 49 miRNAs (16 upregulated and 33 downregulated) were differentially expressed in glioma tissues, and miR-339-5p was the most downregulated. The clone number, invasion number, and healing rate of cells in miR-339-5p mimic group were decreased compared with miR-NC group ( P < 0.05 ); the clone quantity, invasion number, and healing rate of cells in miR-339-5p inhibitor group were increased compared with miR-NC group ( P < 0.05 ). The apoptosis rate of human glioma U87 cells in miR-339-5P mimic group was compared with miR-NC group ( P < 0.05 ); the apoptosis rate of human glioma U87 cells in miR-339-5p suppressor group decreased compared with miR-NC group ( P < 0.05 ). Compared with miR-NC group, the protein expression of Twist, Snsnail, N-cadherin, and Vimentin in miR-339-5p mimic group was considerably decreased, whereas E-cadherin was elevated ( P < 0.05 ). Compared with miR-NC group, the protein expression of Twist, Snsnail, N-cadherin, and Vimentin in miR-339-5p suppressor group was considerably increased, whereas E-cadherin was considerably decreased ( P < 0.05 ). Conclusion. Forty-nine glioma-related miRNAs were screened out, and miRNA expression was significantly different between glioma and normal tissues. The downregulated miR-339-5p in glioma can regulate the proliferative, apoptotic, invasive, and migratory abilities of glioma U87 cells and might suppress the occurrence and development of glioma.

Objective. Finding miR-339-5p inhibitory functions in glioma through PTP4A1/HMGB1 pathway. Methods. From May 2020 to August 2021, 20 glioblastoma and para cancer tissues were chosen for qRT-PCR analysis. The miR-NC, miR-con, miR-339-5PMIMIC, and miR-con + groups were transfected into human glioma U251 cells. The capacity of cell vascular-like structure construction was found by simulating angiogenesis, and the ability of cell movement was examined by cell scratching. The twofold luciferase reporter gene method determined that miR-339-5p targets PTP4A1, and the protein expression levels of PTP4A1 and HMGB1 were examined using Western blot. Results. MiR-339-5P expression was substantially lower in cancer samples than noncancer samples ( P < 0.05 ). PTP4A1 expression in cancer samples was higher than in healthy controls ( P < 0.05 ). The miR-339-5p group produced significantly less vascular-like structures than the NC and miR-con groups ( P < 0.05 ). The miR-339-5p group lowered the invasive index and migratory rate of U251 cells ( P < 0.05 ). PTP4A1 inhibited the luciferase activity of the pTP4A1-WT reporter gene ( P < 0.05 ) but not the PTP4A1-MUT ( P > 0.05 ). The miR-339-5p group had lower protein levels of PTP4A1 and HMGB1 than the NC and miR-con groups ( P < 0.05 ). The development of vascular-like structures was substantially more significant in the miR-con +PTP4A1 group than in the miR-con and miR-339-5p +PTP4A1 groups ( P < 0.05 ). In terms of migration and invasion index, there was a substantial difference between the miR-339-5p +PTP4A1 and the miR-con +PTP4A1 groups ( P < 0.05 ). The miR-con +PTP4A1 group had a greater migration rate and invasive index than the miR-con and miR-339-5p +PTP4A1 groups ( P < 0.05 ). Conclusion. MiR-339-5P inhibits angiogenic mimicry, migration, and invasion of brain glioma U251 cells by inhibiting the PTP4A1/HMGB1 signal pathway.